Oxidative damage and vital rates in the copepod Acartia tonsa in subtropical estuaries with contrasting anthropogenic impact

- Higher protein carbonylation under experimental conditions of anthropogenic impact
- The actin was identified as a specific target of carbonylation.
- Vital rates were not affected under conditions of high anthropogenic impact.
- The existence of a critical threshold of protein damage is proposed.
- Below that threshold, vital rates are resilient to oxidative damage.

Oxidative damage occurs as a natural process in organisms, but recently several studies suggested that oxidative damage may be enhanced by environmental stress. Here, levels of oxidative damage (protein carbonylation) and vital rates performances of Acartia tonsa were compared in two estuaries with different degree of anthropogenic impact through field and experimental approaches. Wild copepods were repeatedly sampled at two contrasting estuarine ecosystems: Laguna de Rocha (low anthropogenic impact) and Montevideo Bay (high anthropogenic impact), and analyzed for protein carbonylation and incidence of dead copepods. In the lab, cultured copepods were kept for 16 days in water from each site and in artificial seawater as control, and analyzed for protein carbonylation, egg production, ingestion rates and egg hatching success. Additionally, it was identified in this species one body protein subjected to carbonylation by mass spectrometry. Protein carbonylation was similar in wild animals from both sites. The incidence of dead copepods differed between sites in all sampling dates, but significant interactions were observed between dates and sites. Experimental results indicated higher protein carbonylation levels in Montevideo Bay treatment (highly impacted site), according to expectations. Mass spectrometry analysis allowed the identification of the actin, as a target of carbonylation. Vital rates showed different patterns: highest egg production rate at Montevideo Bay treatment, but similar egg hatching success and ingestion rate between treatments. This work provides evidence partially consistent with the hypothesis that predicts an enhancement of oxidative stress under degraded environmental conditions, further identifying an ubiquitous and highly functionaly significant protein, the actin, as a specific target of damage.